Causes, lab diagnosis, and clinical significance of iron deficiency anemia

on 4.3.09 with 0 comments



  • Fe deficiency is the most frequent nutritional d/o worldwide

  • Most of the Fe is absorbed in the duodenum, and Fe balance is largely maintained by regulation of absorptive intake

  • Forms of Fe in the body

    • Functional components

      • About 80% is in Hb

      • Mb and Fe-containing enzymes like catalase and cytochromes contain the rest

    • Storage components

      • Ferritin

        • Protein-Fe complex in liver, spleen, marrow, and skeletal muscle

        • In the liver, most of the ferritin is found in the parenchyma and comes from plasma transferrin

        • Elsewhere, ferritin is found in the macrophages and mostly comes from the breakdown of senescent or damaged RBCs

        • Serum [ferritin] is a good reflection of body Fe stores, but it is an acute phase reactant and it can become elevated with acute inflammation, even with Fe dietary deficiency

      • Hemosiderin

        • Located in lysosomes

        • This is what is mostly stained by special Fe stains (e.g., Prussian blue)

  • Causes of (-) Fe balance and anemia

    • Inadequate intake, poor absorption (e.g., sprue, gastrectomy), excessive demand (e.g., pregnancy), or chronic blood loss

    • Chronic blood loss is the most frequent cause in the US and this includes excessive menstrual losses and GI tract loss from ulcers and tumors

  • Effects of Fe deficiency are sequential

    • Depletion of storage Fe, followed by decreased serum [Fe] and decreased transferrin saturation (it’s normally 33% saturated), which will show up as a high total plasma Fe-binding capacity

    • Marrow sideroblasts disappear, leading to a microcytic, hypochromic anemia

    • Decreased Hb synthesis leads to elevation of free erythrocyte protoporphyrin (may help tell Fe deficiency from other causes of microcytosis, such as thalassemias and anemia of chronic disease

  • Depletion of Fe-containing enzymes may lead to koilonychias, alopecia, and atrophy of the tongue and GI tract mucosa, leading to malabsorption

  • Plummer-Vinson syndrome: Fe deficiency anemia, atrophic glossitis and esophageal webs

Category: Medical Subject Notes , Pathology Notes

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